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July 1967

Experimental Uremic Encephalopathy: Permeability and Electrolyte Metabolism of Brain and Other Tissues

Author Affiliations

New York
From the Department of Neurology and Neurological Clinical Research Center, College of Physicians and Surgeons, Columbia University and Neurological Institute, Presbyterian Hospital, New York. Dr. Raskin is presently at the National Institutes of Health, Bethesda, Md. Dr. Fishman is now at the University of California Medical Center, San Francisco.

Arch Neurol. 1967;17(1):10-21. doi:10.1001/archneur.1967.00470250014002

CLINICAL experience with the artificial kidney has established that toxic factors responsible for uremic encephalopathy are readily dialyzable, and thereby the neurological manifestation of uremia may be reversed rapidly. Despite greater sophistication in the management of renal insufficiency, the pathophysiology of the encephalopathy is poorly understood, and analyses of brain with traditional neuropathological techniques have failed to yield any specific structural correlations.1 Therefore, an experimental model of uremia was established in rats in order to characterize physiologically the encephalopathy in terms of several aspects of brain metabolism. Permeability of brain and other tissues was studied, using two nonmetabolized sugars, inulin14C (molecular weight 5,000) and sucrose14C (mol wt 342), and sulfate35S, when the latter was corrected for metabolic incorporation into plasma and brain.2 Sodium24 and potassium42 transfers were studied because of their pertinence to neural function, and the enzyme,

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